Hepatic fibrosis is examined in mice infected with schistosome species pathogenic for man. Mouse strains developed markedly different degrees of hepatic fibrosis following infection with S. mansoni. Among inbred strains, Nmri mice showed maximal fibrosis and C57BL/6 mice minimal fibrosis. Inheritance was multigenic with incomplete dominance. Granuloma size also differed markedly between the mouse strains and was also inherited in an incompletedly dominant fashion with several genes apparently involved. In backcross generations hepatic fibrosis and granuloma size segregated independently. S. japonicum infections in different mouse strains also induced variable fibrosis and the relative rank of the mouse strains was similar to that for S. mansoni; however some mouse strains (e.g. C57BL/6 having small granulomas in S. mansoni infection had large granulomas after S. japonicum infection and granuloma size was clearly not related to fibrosis. Mice without antibody (anti-u treated) formed normal granulomas around both S. mansoni and s. japonicum eggs at 7-8 weeks after infection. T cell deficient (nude) mice formed discreet granulomas around S. japonicum eggs but the lesions were much smaller than those in heterozygotes and fibrosis was minimal. Thus, contrary to expectations, T cells are much more important than antibody in the formation of S. japonicum egg granulomas and the necrotizing features of the granulomas were not antibody dependent.